We have shown that antibodies raised against anti-human, plasma fibronectin are capable to stimulating platelets to secrete the contents of their dense granules. We have obtained antibodies from rabbits, a goat, and three lines of mouse hybridoma. We have found that the platelets from some human donors are stimulated by the rabbit antibody but not goat antibody, some stimulated by goat antibody but not rabbit antibody, some by neither antibody, and some by both antibodies. Two lines of monoclonal antibodies stimulated the platelets of all donors, while those from one line stimulated no donor's platelets. We postulated that only a portion of fibronectin on the membrane of platelets is exposed to the action of antibodies and that this portion carries some genetically determined differences amongst the platelet fibronectin from different donors as well as a small (or antigenically weak) portion which is genetically constant. We will carry out determinations of antibody binding to platelets of different donors, determinations of the portion of the fibronectin molecule which shows genetic differences, and determine the location of the antigenic sites to the monoclonal antibodies.